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Acute Decompensated Heart Failure
An overweight middle-aged man presented with acute shortness of breath, elevated blood pressure, coarse lung sounds, low oxygen saturation, and leg swelling. His initial evaluation found signs of severe congestive heart failure including pulmonary edema. Further assessment is needed to determine the underlying cause, guide treatment, and classify the type and severity of heart failure.
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Acute Decompensated Heart Failure
- 1. TEXT ACUTE DECOMPENSATED HEARTFAILURE ▸Ingo Moeller ▸SCGH Registrar Teaching 08/06/2017
- 2. ACUTE DECOMPENSATED HEARTFAILURE CLINICAL VIGNETTE - MY PATIENT FROM SATURDAY NIGHT Its 6:32 am and you are the Registrar in charge of the Saturday night shift at Charlie’s. You are tired after battling through Amphetamine and ETOH inebriated Patients, its quiet, ….too quiet! “Its quite quiet” the Intern says…… and 2 minutes later SJA rushes a patient into T2. The patient is an overweight middle-aged man who is also struggling to breathe. SJA report that his blood pressure was 220/130 mm Hg at the scene. Shifty immediately attaches the patient to the cardiac monitor and obtains vital signs. His blood pressure is now 240/140 mm Hg. HR is 140. You listen to his lungs and notice coarse, wet breath sounds. Your patient is tachypnoeic, sweaty, leaning forward in bed, and saturating 72% on room air. His oxygen saturation improves to 88% on a 100% nonrebreather mask. His legs are oedematous, and he has marked conversational dyspnea(single words). Respiratory arrest seems certain unless appropriate action is taken, and you wonder what to do…..
- 3. ACUTE DECOMPENSATED HEARTFAILURE INTRODUCTION….. ACUTE DECOMPENSATED HEART FAILURE ▸incidence of in-hospital mortality among patients admitted to the hospital for decompensated heart failure is 6.4% ▸in individuals aged 65 to 69 years, the prevalence of heart failure is roughly 20 per 1000, ▸Among people >65 years of age presenting to primary care with breathlessness on exertion, one in six will have unrecognized HF (mainly HFpEF) ▸prevalence jumps to more than 80 per 1000 in individuals older than 85 years.
- 4. ACUTE DECOMPENSATED HEARTFAILURE ACUTE HEART FAILURE ▸Acute heart failure (AHF) is a relevant public health problem causing the majority of unplanned hospital admissions in patients aged of 65 years or more. ▸AHF was historically described as a pump failure with downstream hypoperfusion and upstream congestion. ▸AHF remain poor with 90-day rehospitalization and 1-year mortality rates reaching 30% Understanding acute heart failure: pathophysiology and diagnosis, Eur Heart J Suppl (2016)
- 5. EPIDEMIOLOGY OF HEART FAILURE(IN THE US) MORE DEATHS FROM HEART FAILURE THAN FROM ALL FORMS OF CANCER COMBINED 550,000 NEW CASES/YEAR 4.7 MILLION SYMPTOMATIC PATIENTS; ESTIMATED 10 MILLION IN 2037 *Rich M. J Am Geriatric Soc. 1997;45:968–974. American Heart Association. 2001 Heart and Stroke Statistical Update. 2000. 3.5 4.7 10 0 2 4 6 8 10 12 1991 2000 2037* HeartFailurePatientsinUS (Millions)
- 6. ACUTE DECOMPENSATED HEARTFAILURE NOT ALL HEART FAILURE IS THE SAME. - Heart failure with preserved ejection fraction (HFpEF) - and heart failure with reduced ejection fraction (HFrEF) - may present with either hypertension or hypotension - represent distinct underlying pathophysiologies that require different approaches in treatment. - HFpEF and HFrEF are equal in terms of occurrence, morbidity, and mortality. Karrowni W, Chatterjee K. Diastolic heart failure: the current understanding and approach for management with focus on intensive care unit patients. J Intensive Care Med. 2014;29(3):119-127. (Review article)
- 7. ACUTE DECOMPENSATED HEARTFAILURE SYSTOLIC AND DIASTOLIC HEART FAILURE Heart failure occurs when the heart is either unable- -to Pump blood during systole (HFrEF) or -to Fill with blood during diastole (HFpEF) Systolic heart failure results in heart failure with reduced ejection fraction. Diastolic heart failure results in heart failure with preserved ejection fractio
- 8. ACUTE DECOMPENSATED HEARTFAILURE HEART FAILURE WITH PRESERVED EJECTION FRACTIONHFpEF is defined as heart failure with ejection fraction that is either borderline (41%- 49%) or normal (> 50%). Diastolic dysfunction is characterised by elevated left ventricular filling pressures with impaired myocardial relaxation. responds differently to traditional heart failure therapies that were intended for the traditional treatment of HFrEF
- 9. ACUTE DECOMPENSATED HEARTFAILURE ETIOLOGY AND PATHOPHYSIOLOGY ▸Injury to Myocardium ▸secondary to a number of causes that develop slowly over time (uncontrolled hypertension, diabetes) or ▸more suddenly (eg, coronary ischaemia, STEMI) ▸Regardless of the cause, myocardial injury results in ▸structural-abnormalities of the ventricular wall that impair systolic contraction or diastolic relaxation ▸electrophysiological, ->impaired conduction,(QRS widening on ECG), which can lead to conduction blocks and re-entrant dysrhythmias and ▸biochemical remodeling -> impaired myocyte functionality and increased risk of dysrhythmia
- 10. ACUTE DECOMPENSATED HEARTFAILURE THE ISSUE IS… ▸Regardless of the underlying aetiology, patients presenting with AHF appear very similar to each other: ▸Sodium and Fluid retention, ▸excess Fluid backing up into the lungs, abdomen, and extremities. ▸The result is fatigue, peripheral oedema, and dyspnea that is often worse with exertion
- 11. ACUTE DECOMPENSATED HEARTFAILURE PATHOPHYSIOLOGY OF ACUTE HEART FAILURE ▸Acute heart failure is defined as new-onset or worsening of symptoms and signs of HF ▸AHF typically includes symptoms or signs related to congestion and volume overload rather than to hypoperfusion ▸level of congestion and the number of congested organs have prognostic relevance in HF patients Gheorghiade M. European Society of Cardiology, European Society of Intensive Care Medicine. Assessing and grading congestion in acute heart failure: a scientific statement from the acute heart failure committee of the heart failure association of the European Society of Cardiology and endorsed by the European Society of Intensive Care Medicine. Eur J Heart Fail 2010
- 12. ACUTE DECOMPENSATED HEARTFAILURE CIRCLING THE DRAIN
- 13. ACUTE DECOMPENSATED HEARTFAILURE PATIENT EVALUATION IN ED ▸history, ▸physical examination, ▸chest radiography, ▸12-lead ECG, ▸Troponin ▸ electrolytes, and a ▸complete blood cell count ▸BNP Collins SP, . Prevalence of negative chest radiography results in the emergency department patient with decompensated heart failure. Ann Emerg Med. 2006;47:13–18.
- 14. ACUTE DECOMPENSATED HEARTFAILURE DIFFERENTIAL DIAGNOSIS ▸look for alternative diagnoses ▸do not miss reversible causes and ▸other life threatening causes
- 15. ACUTE DECOMPENSATED HEARTFAILURE CAUSES OF AHF
- 16. ACUTE DECOMPENSATED HEARTFAILURE PRECIPITANTS AND DIFFERENTIAL DIAGNOSIS ▸Differential Diagnosis for Patients Presenting With Dyspnea ▸Life-Threatening causes ▸Decompensated heart failure ▸Chronic obstructive pulmonary disease ▸ Asthma ▸Pneumonia ▸Pulmonary embolism ▸Acute coronary syndromes ▸Aortic dissection ▸Pericarditis or pericardial effusion ▸Pneumothorax ▸Precipitants of Acute heart failure ▸Acute coronary ischaemia ▸Valvular dysfunction ▸Cardiac arrhythmia ▸Pulmonary embolism ▸Myocarditis ▸Hypertensive emergency ▸Pericardial tamponade ▸Severe anemia ▸Worsening renal failure ▸Sepsis ▸Drug noncompliance ▸Dietary indiscretion ▸Medication side effect / change ▸Thyroid dysfunction
- 17. ACUTE DECOMPENSATED HEARTFAILURE HISTORY TAKING PEARLS ON SEVERITY OF UNDERLYING DISEASE ▸Expect more severe disease in Patients with ▸AICD or PPM (automated implantable cardioverter defibrillator ▸Medication clues e.g. Patient on Spironolactone ▸Patients on homeopathic doses of Beta Blockers or ACE might have baseline low BP ▸whilst patients with big doses are truely Hypertensive’s at baseline ▸Weight change if known?
- 18. ACUTE DECOMPENSATED HEARTFAILURE AHF - SIGNS AND SYMPTOMS ▸Exertional dyspnea and/or dyspnea at rest ▸Orthopnea ▸Acute pulmonary oedema ▸Chest pain/pressure and palpitations ▸Tachycardia ▸Fatigue and weakness ▸Nocturia and oliguria ▸Anorexia, weight loss, nausea ▸Exophthalmos and/or visible pulsation of eyes ▸Distention of neck veins ▸Weak, rapid, and thready pulse ▸Rales, wheezing ▸S 3 gallop and/or pulsus alternans ▸Increased intensity of P 2 heart sound ▸Hepatojugular reflux ▸Ascites, hepatomegaly, and/or anasarca ▸Central or peripheral cyanosis, pallor ▸Big Ticket items: ▸Patient Position ▸Hypertensive/Hypotensive ▸Distention of neck veins - Surrogate for Right Heart pressure ▸Auscultation —>Rales, wheezing - worse rales>worse AHD ▸New Heart Murmur / Distant Heart sound ▸S 3 gallop - Diagnostic for AHD ▸uni/bilateral Leg swelling
- 19. ACUTE DECOMPENSATED HEARTFAILURE ASSESSMENT OF HF PROBABILITY ▸1. Clinical history: ▸History of CAD (MI, revascularization) ▸History of arterial hypertension ▸Exposition to cardiotoxic drug/radiation ▸Use of diuretics ▸Orthopnoea / paroxysmal nocturnal dyspnoea ▸2. Physical examination: ▸Rales ▸Bilateral ankle oedema ▸Heart murmur ▸Jugular venous dilatation ▸Laterally displaced/broadened apical beat ▸3. ECG: ▸Any abnormality
- 20. ACUTE DECOMPENSATED HEARTFAILURE ASSESSMENT OF HEART FAILURE PROBABILITY ▸1. Clinical history; 2. Physical examination; 3. ECG ▸≥1 present ▸NATRIURETIC PEPTIDES ▸NT-proBNP ≥125 pg/mL ▸BNP ≥35 pg/mL ▸Consider aetiology and start appropriate treatment ▸ECHOCARDIOGRAPHY
- 21. ACUTE DECOMPENSATED HEARTFAILURE ESC HEART FAILURE GUIDELINES ▸Use transthoracic echocardiography in patients with suspected or established HF for the assessment of myocardial structure and function along with the measurement of LVEF to establish the diagnosis of ▸HF with reduced (HFrEF, LVEF<40%), ▸mid-range (HFmrEF, LVEF: 40-49%) or ▸preserved ejection fraction (HFpEF, LVEF≥50%)
- 22. ACUTE DECOMPENSATED HEARTFAILURE CLINICAL CLASSIFICATION
- 23. ACUTE DECOMPENSATED HEARTFAILURE FORRESTER HAEMODYNAMIC SUBSETS - AHF IN NUMBERS Subset Description I: Warm and dry (normal) PCWP 15–18 mmHg and CI >2.2 L/min/m2 II: Warm and wet (congestion) PCWP >18 mmHg and CI >2.2 L/min/m2 III: Cold and dry (hypoperfusion) PCWP 15–18 mmHg and CI <2.2 L/min/m2 IV: Cold and wet (congestion and hypoperfusion) PCWP >18 mmHg and CI <2.2 L/min/m2 Forrester Hemodynamic Subsets CI: cardiac index; PCWP: pulmonary capillary wedge pressure. Forrester JS, Diamond G, Chatterjee K, et al. Medical therapy of acute myocardial infarction by application of hemodynamic subsets. N Engl J Med. 1976;295:1356–1362.
- 24. ACUTE DECOMPENSATED HEARTFAILURE BEDSIDE TEST - ECG
- 25. ACUTE DECOMPENSATED HEARTFAILURE ECG - INFERIOR STEMI WITH RV INFARCTION ST elevation in V1 – the only standard ECG lead that looks directly at the right ventricle. ST elevation in lead III > lead II – because lead III is more “rightward facing” than lead II and hence more sensitive to the injury current produced by the right ventricle. Right ventricular infarction complicates up to 40% of inferior STEMIs. Patients with RV infarction are very preload sensitive (due to poor RV contractility) and can develop severe hypotension in response to nitrates or other preload-reducing agents. Hypotension in right ventricular infarction is treated with cautious fluid loading, and nitrates are contraindicated.
- 26. ACUTE DECOMPENSATED HEARTFAILURE IMAGING IN AHF ▸ CXR ▸ ECHOCARDIOGRAPHY ▸ LUNG ULTRASOUND
- 27. ACUTE DECOMPENSATED HEARTFAILURE RADIOLOGICAL FEATURES OF ACUTE PULMONARY OEDEMA ▸There are distinct radiological phases. ▸Interstitial phase is the fluid filling up spaces between acini; ▸the alveolar phase is where that fluid floods the air spaces. ▸Interstitial pulmonary oedema may develop first. ▸Small pulmonary vessels lose their definition ▸Peribronchial cuffing occurs: ▸Kerley B lines ▸Thickening of fissures ▸Pleural effusions ▸Bat Wing" oedema ▸15% Normal CXR
- 28. ACUTE DECOMPENSATED HEARTFAILURE RADIOLOGICAL STAGES OF HEART FAILURE
- 29. ACUTE DECOMPENSATED HEARTFAILURE MILD PULMONARY CONGESTION WITH CEPHALISATIONAP chest radiograph demonstrates cephalisation (upper lobe vascular redistribution) in stage I CCF where there is elevation of the left atrial pressure 10-15 mmHg. Normal left atrial pressure is 5-10 mmHg. http://www.radiologyassistant.nl/en/p4c132f36513d4
- 30. ACUTE DECOMPENSATED HEARTFAILURE MORE ADVANCED CONGESTION - KERLEY B LINES Stage II - Interstitial oedema Stage II of CHF is characterised by fluid leakage into the interlobular and peribronchial interstitium as a result of the i When fluid leaks into the peripheral interlobular septa it is seen as Kerley B or septal lines. Kerley-B lines are seen as peripheral short 1-2 cm horizontal lines near the costophrenic angles. These lines run perpendicular to the pleura.
- 31. ACUTE DECOMPENSATED HEARTFAILURE EVEN MORE ADVANCED CONGESTION When fluid leaks into the peribronchovascular interstitium it is seen as thickening of the bronchial walls (peribronchial cuffing) and as loss of definition of these vessels (perihilar haze). On the left a patient with heart failure. There is an increase in the caliber of the pulmonary vessels and they have lost their definition because they are
- 32. ACUTE DECOMPENSATED HEARTFAILURE ENDSTAGE - PULMONARY CONGESTION WITH CARDIOMEGALY
- 33.
- 34. ACUTE DECOMPENSATED HEARTFAILURE ECHOCARDIOGRAPHY ▸ Primary imaging modality to evaluate a patient’s cardiac function and evaluate for either systolic or diastolic dysfunction ▸ only part of the initial ED examination where systolic and diastolic dysfunction can be distinguished ▸ approximation of LVEF ▸ visual assessment that looks for the general quality of the “heart’s squeeze”
- 35. ACUTE DECOMPENSATED HEARTFAILURE ECHOCARDIOGRAPHY ▸ A more precise way to examine left ventricular ejection fraction is via E-point septal separation (EPSS), ▸ measures the smallest distance between the tip of the mitral leaflet and the interventricular septum during diastole. ▸ This distance is assessed using M-mode, with the indicator overlying the tip of the mitral lea et. ▸ The larger this distance, the lower the ejection fraction. EPSS > 7 mm is indicative of poor left ventricular Secko MA, Lazar JM, Salciccioli LA, et al. Can junior emer- gency physicians use E-point septal separation to accurately estimate left ventricular function in acutely dyspneic pa- tients? Acad Emerg Normal Normal Abnormal M-Mode
- 36. ACUTE DECOMPENSATED HEARTFAILURE PULMONARY ULTRASOUND - B LINES Multiple B-lines from a case of cardiogenic pulmonary oedema. When a similar pattern is visualised on multiple locations in the anterior and lateral chest, it is diagnostic of the interstitial syndrome. Interstitial Pulmonary fluid is identifiable on ultrasound as vertical hyper-echoic lines that arise from, and run perpendicular to, the pleura. These lines extend into the lung parenchyma and are referred to as B-lines. The presence of 3 or more B-lines in at least 2 bilateral lung zones is indicative of pulmonary oedema. The greater the number of zones demonstrating B-lines, the higher the likelihood of ADHF Combined with BNP - High Dx accuracy! Liteplo AS, et al. Emergency thoracic ultrasound in the differentiation of the etiology of shortness of breath (ETUDES): sonographic B-lines and N-terminal pro-brain-type natriuretic peptide in diagnosing congestive heart failure. Acad
- 37. ACUTE DECOMPENSATED HEARTFAILURE INITIAL EVALUATION - LABORATORY TESTING ▸BNP ▸Troponin ▸FBC ▸U/E’s ▸Supplementary Testing
- 38. ACUTE DECOMPENSATED HEARTFAILURE BNP ▸BNP Cutoff of 100 ng/l, ▸BNP had a sensitivity 90%, specificity 76%, negative predictive 79%, and positive predictive value of 89%. ▸In this capacity, BNP is highly useful to exclude AHF ▸negative likelihood ratio of BNP at 100 pg/mL is 0.13 -LR ▸< 100 ng/l strongly suggestive against AHF ▸>400ng/l suggestive of AHF exacerbation • However may be falsely elevated in: • Renal disease, atrial fibrillation, pulmonary HTN • May be falsely low in: • Obese patients, HFPEF • High BNP increased Mortality in men 1. Maisel AS, et all . Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med. 2002;347:161–167.
- 39. ACUTE DECOMPENSATED HEARTFAILURE TROPONIN ▸Useful for risk stratification ▸? underlying primary cause of AHF (cardiac strain, ischaemia, infarction) ▸elevated trop = increased in hospital mortality 8% versus 2.7 % if Neg Trop ▸increased re-hospitalisation rate ▸increased risk at death at 90 days
- 40. ACUTE DECOMPENSATED HEARTFAILURE FBC, U/E,S + SUPPLEMENTAL TESTS ▸Anaemia- HB under 8 (in IHD under 10)- improve Oxygen carrying capacity by transfusion ▸Sodium and Renal function (AKI?-end organ damage) ▸Liver function (end organ damage) ▸Thyroid function (cause of failure?) ▸Calcium - low? improves cardiac contractility ▸amyloidosis, pheochromocytoma etc as rare causes.
- 41. ACUTE DECOMPENSATED HEARTFAILURE TREATMENT AIMS ▸Decrease left ventricular diastolic pressure, by decreasing systemic vascular resistance and improving systolic and diastolic functional reserve. ▸Promote coronary blood flow. ▸Correct acute respiratory failure. ▸In-hospital mortality for APO is up to 12%, with one-year mortality up to 40% !
- 42. ACUTE DECOMPENSATED HEARTFAILURE MANAGEMENT OF PRELOAD ▸ Diuretics ▸ Fluid restriction ▸ Venodilators ▸ Aldosterone agonists ▸ Beta-blockers ▸ Maintenance of sinus rhythm and atrial systolic contribution ▸ Pacing to maintain AV synchrony
- 43. ACUTE DECOMPENSATED HEARTFAILURE MANAGEMENT OF AFTERLOAD ▸Left ventricle ▸Vasodilators ▸ACE-inhibitors ▸Beta-blockers ▸Right ventricle ▸Normoxia ▸Normocapnea ▸Avoidance of excessive postive respiratory pressures ▸Pulmonary vasodilators
- 44. ACUTE DECOMPENSATED HEARTFAILURE MANAGEMENT OF CARDIAC CONTRACTILITY ▸ Inotropes ▸Digoxin ▸Dobutamine ▸Levosimendan ▸ Cardiac resychronisation ▸ Supportive hormones and micronutrients (cortisol, insulin, calcium, glucagon, thyroxine, thiamine etc
- 45. ACUTE DECOMPENSATED HEARTFAILURE DIAGNOSIS AND INITIAL PROGNOSTIC EVALUATION - BE A CHAMP Jessup, M. et al. (2016) 2016 ESC and ACC/AHA/HFSA heart failure guideline update — what is new and why is it important? Nat. Rev. Cardiol. doi:10.1038/nrcardio.2016.134
- 46. ACUTE DECOMPENSATED HEARTFAILURE IDENTIFICATION OF PRECIPITANTS/CAUSES LEADING TO DECOMPENSATION THAT NEEDS URGENT MANAGEMENT ▸ Acute coronary syndrome. ▸ Coexistence of these two clinical conditions (ACS and AHF) always identifies a very-high-risk group where an immediate (i.e. <2 h from hospital admission in patients with NSTEMI, analogous to STEMI management) ▸ invasive strategy with intent to perform revascularization is recommended, irrespective of ECG or biomarker findings. ▸ Hypertensive emergency. ▸ AHF precipitated by rapid and excessive increase in arterial blood pressure typically manifests as acute pulmonary oedema. Aggressive blood pressure reduction (in the range of 25% during the first few hours and cautiously thereafter) with i.v. vasodilators in combination with loop diuretics is recommended. ▸ Rapid arrhythmias or severe bradycardia/conduction disturbance. ▸ Severe rhythm disturbances in patients with AHF and unstable conditions should be corrected urgently with medical therapy, electrical cardioversion or temporary pacing ▸ Electrical cardioversion is recommended if an atrial or ventricular arrhythmia is thought to be contributing to the patient's haemodynamic compromise in order to restore sinus rhythm and improve the patient's clinical condition. ▸ Acute mechanical cause underlying AHF. ▸ mechanical complication of ACS (free wall rupture, ventricular septal defect, acute mitral regurgitation), ▸ chest trauma or cardiac intervention ▸ Echocardiography is essential for diagnosis, and treatment typically requires circulatory support with surgical or percutaneous intervention. ▸ • Acute pulmonary embolism. When acute pulmonary embolism is confirmed as the cause of shock or hypotension, immediate specific treatment is recommended with primary reperfusion either with thrombolysis, catheter-based approach or surgical embolectomy.
- 47. ACUTE DECOMPENSATED HEARTFAILURE INITIAL MANAGE MENT PATHWAY
- 48. ACUTE DECOMPENSATED HEARTFAILURE 5 DISTINCT TREATMENT GROUPS ▸ Acute heart failure syndrome (AHFS) spectrum can be divided into 5 groups as regards therapeutic management: ▸Dyspnoea + /- congestion with elevated systolic blood pressure (SBP)>140 mmHg, usually with abrupt onset APO (most frequent type) ▸Dyspnoea + /- congestion with normal SBP 100-140 mmHg, usually with gradual onset predominant systemic oedema and milder APO ▸Dyspnoea + /- congestion with low SBP <100 mmHg, with predominant cardiogenic shock or end-stage cardiac failure (most fatal type) ▸Dyspnoea + /- congestion with signs of ACS such as chest pain ▸Isolated RV failure usually without APO Mebazza A, Gheoghiade M, Pina I et al. Practical recommendations for pre- hospital and early in-hospital management of patients presenting with acute heart failure. Crit Care Med 2008;36:S129-39.
- 49. ACUTE DECOMPENSATED HEARTFAILURE CLINICAL CLASSIFICATION Classification of patients presenting with acutely decompensated heart failur Yancy C W et al. Circulation. 2013;128:e240-e327
- 50. ACUTE DECOMPENSATED HEARTFAILURE PRACTICAL RECOMMENDATION Alexandre Mebazaa, MD, PhD et all “Practical recommendations for prehospital and early inhospital management of patients presenting with acute heart failure syndromes” Crit Care Med 2008 Vol. 36, No. 1
- 51. ACUTE DECOMPENSATED HEARTFAILURE INITIAL MANAGE MENT PATHWAY
- 52. ACUTE DECOMPENSATED HEARTFAILURE VASODILATORS ▸ Safety of high dose initial GTN: ▸ 800 mcg(2x0,4mg sl tab) GTN sl if BP>180mmHg ▸ 1200 mcg(3x0.4mg sl Tab) for BP>200 mmHg ▸ only 3/75 incidence of Hypotension ▸ Initial GTN dose iv 50-100mcg/min up to 400mcg/min for 2 min max with Physician in attendance ▸ Vasodilators should be used with extreme caution in patients with significant mitral or aortic stenosis. Clemency BM, Thompson JJ, Tundo GN, et al. Prehospital Disaster Medicine high-dose sublingual nitroglycerin rarely causes hypoten- sion. Prehosp Disaster Med. 2013;28(5):477-481. (Retrospective cohort study; 75 patients)
- 53. ACUTE DECOMPENSATED HEARTFAILURE VASODILATORS ‣ No robust evidence confirming their beneficial effects. ‣ They have dual benefit by ‣ decreasing venous tone (to optimize preload) ‣ decreasing arterial tone (decrease afterload). ‣ they may also increase stroke volume. ‣ Vasodilators are especially useful in patients with hypertensive AHF, whereas in SBP <90 mmHg (or with s
- 54. ACUTE DECOMPENSATED HEARTFAILURE INOTROPIC AGENTS ▸ Digoxin - no improvement over placebo in one (older) study ▸ Dopamine was compared with norepinephrine in the treatment of various shock patients. ▸ Increased Mortality ▸ A subgroup analysis suggested that norepinephrine would have fewer side effects and lower mortality ▸ Norepinephrine 1st choice but increasing Oxygen demand in Heart De Backer D , Biston P, Devriendt J, Madl C, Chochrad D, Aldecoa C, Brasseur A, Defrance P, Gottignies P, Vincent J-L. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med 2010;362:779–789.
- 55. ACUTE DECOMPENSATED HEARTFAILURE INOTROPES
- 56. ACUTE DECOMPENSATED HEARTFAILURE DIGOXIN ▸Digoxin is if at all indicated in patients with AF and rapid ventricular rate (>110 bpm) ▸boluses of 0.25–0.5 mg i.v. if not used previously
- 57. ACUTE DECOMPENSATED HEARTFAILURE MANAGEMENT OF PATIENTS WITH CARDIOGENIC SHOCK ▸Pharmacologic therapy aims to improve organ perfusion ▸by increasing cardiac output and blood pressure. ▸fluid challenge, ▸inotropic agent (Dobutamine)and a ▸vasopressor (noradrenaline) as needed. ▸immediate Coronary Angiogram recommended
- 58. ACUTE DECOMPENSATED HEARTFAILURE DIURETICS ▸Diuretics are a cornerstone in the treatment of patients with AHF and signs of fluid overload and congestion. ▸Diuretics increase renal salt and water excretion and have some vasodilatory effect. ▸In patients with AHF and signs of hypoperfusion, diuretics should be avoided before adequate perfusion is attained. ▸The initial approach to congestion management involves i.v. diuretics with the addition of vasodilators for dyspnoea relief if blood pressure allows. ▸Options include dual nephron blockade by loop diuretics (i.e. furosemide or torasemide) with thiazide diuretics or natriuretic doses of MRAs ▸Administration of furosemide at 2.5 times the previous oral dose resulted in greater improvement in dyspnoea, larger weight change and fluid loss at the cost of transient worsening in renal function. ▸patients with new-onset AHF or those with chronic HF without a history of renal failure and previous use of diuretics may respond to i.v. boluses of 20–40 mg
- 59. ACUTE DECOMPENSATED HEARTFAILURE FURUSEMIDE Felker GM , Lee KL, Bull DA, Redfield MM, Stevenson LW, Goldsmith SR, LeWinter MM, Deswal A, Rouleau JL, Ofili EO, Anstrom KJ, Hernandez AF, McNulty SE, Velazquez EJ, Kfoury AG, Chen HH, Givertz MM, Semigran MJ, Bart BA, Mascette AM, Braunwald E, O'Connor CM. Diuretic strategies in patients with acute decompensated heart failure. N Engl J Med 2011;364:797–805. ▸In Patient with Evidence of Fluid overload Diuretics to be started early in ED stay ▸In the ‘high-dose’ arm of the DOSE study, administration of furosemide at 2.5 times the previous oral dose resulted in greater improvement in dyspnoea, larger weight change and fluid loss at the cost of transient worsening in renal function ▸i.v. Furusemide should be given at least the same or larger the daily po dose to improve outcomes. ▸starting does for Furusemide in de move patients 20-40mg iv
- 60. ACUTE DECOMPENSATED HEARTFAILURE OXYGEN ▸In AHF, oxygen should not be used routinely in non- hypoxaemic patients, as it causes vasoconstriction and a reduction in cardiac output. ▸ In COPD, hyperoxygenation may increase ventilation– perfusion mismatch, suppressing ventilation and leading to hypercapnia. ▸During oxygen therapy, acid–base balance and transcutaneous SpO2 should be monitored. Park JH , Balmain S, Berry C, Morton JJ, McMurray JJV. Potentially detrimental cardiovascular effects of oxygen in patients with chronic left ventricular systolic dysfunction. Heart 2010;96:533–538.
- 61. ACUTE DECOMPENSATED HEARTFAILURE OPIATES…RATHER USE BENZO’S ▸Opiates relieve dyspnoea and anxiety. ▸In AHF, routine use of opiates is not recommended and they may only be cautiously considered in patients with severe dyspnoea, mostly with pulmonary oedema. ▸Dose-dependent side effects include nausea, hypotension, bradycardia and respiratory depression (potentially increasing the need for invasive ventilation). ▸There are controversies regarding the potentially elevated mortality risk in patients receiving morphine Peacock WF , Hollander JE, Diercks DB, Lopatin M, Fonarow G, Emerman CL. Morphine and outcomes in acute decompensated heart failure: an ADHERE analysis. Emerg Med J 2008;25:205–209.
- 62. ACUTE DECOMPENSATED HEARTFAILURE LEVOSIMENDAN ▸“Calcium-sensitiser” ▸works by increasing myocardial contractility ▸by sensitising the cardiac myocytes to calcium ▸ In the REVIVE study levosimendan, when added to standard therapy, resulted in a more rapid symptomatic improvement when compared to placebo with standard therapy; ▸increased risk of hypotension and dysrhythmias associated with its administration Packer M, Colucci W, Fisher L, et al. Effect of Levosimendan on the short term clinical course of patients with acutely decompensated heart failure. JACC Heart Fail2013;1(2):103- 111. (Randomized controlled trial; 700 patients
- 63. ACUTE DECOMPENSATED HEARTFAILURE VENTILATORY ASSISTANCE ▸Non-invasive ventilation (NIV) refers to CPAP; or bilevel positive airway pressure (BiPAP) non-invasive pressure support ventilation (NIPSV), where IPAP – EPAP (≡PEEP) reflects the amount of pressure support delivered. ▸CPAP reduces mortality (RR 0.64) and need to intubate (RR 0.44), with no effect on incidence of new MI. BiPAP reduces need to intubate (RR 0.54), but not mortality or new MI. Thus CPAP preferred in APO due to AMI / ischaemia. ▸Note 3CPO trial findings showed negative effect of NIV compared to standard medical therapy alone, but may be explained by sickest patients were excluded, low overall rates of intubation, ischaemia and mortality (i.e. their patients were different), and considerable treatment group crossover after first 2 hours.
- 64. ACUTE DECOMPENSATED HEARTFAILURE NIV ▸Non-invasive positive pressure ventilation includes both CPAP and bi-level positive pressure ventilation (PPV). Bi-level PPV also allows inspiratory pressure support that improves minute ventilation and is especially useful in patients with hypercapnia, most typically COPD patients. ▸Non-invasive positive pressure ventilation includes both CPAP and bi-level positive pressure ventilation (PPV). Bi-level PPV also allows inspiratory pressure support that improves minute ventilation and is especially useful in patients with hypercapnia, most typically COPD patients. ▸Non-invasive positive pressure ventilation reduces respiratory distress and may decrease intubation and mortality rate ▸In one study (Emerg Med J 2004; 21:155-161) survival to hospital discharge was improved with CPAP (10 mm/Hg) over BiPap (Ipap 15 Epap 5) and conventional therapy Vital FMR , Ladeira MT, Atallah AN. Non-invasive positive pressure ventilation (CPAP or bilevel NPPV) for cardiogenic pulmonary oedema. Cochrane Database Syst Rev 2013;5:CD005351.
- 65. ACUTE DECOMPENSATED HEARTFAILURE EARLY REVASCULARISATION THERAPY IN ISCHAEMIC ECG ▸The SHOCK Trial showed a 67% relative improvement in long-term survival, measured at 6 years, for patients managed with rapid revascularization. ▸Role of revascularization is not clear for patients presenting with failure without obvious acute ischemia. Hochman JS, Sleeper LA, Webb JG, et al. Early revasculariza- tion and long- term survival in cardiogenic shock complicat- ing acute myocardial infarction. JAMA. 2006;295(21):2511- 2515. (Randomized controlled trial; 302 patients)
- 66. ACUTE DECOMPENSATED HEARTFAILURE ULTRAFILTRATION ▸Ultrafiltration is similar to hemodialysis; however, it focuses on fluid removal rather than solute exchange. ▸can be accomplished through a smaller-diameter catheter than hemodialysis, but it generally requires a peripherally inserted central catheter (PICC) line ▸The UNLOAD trial evaluated ultrafiltration versus IV diuretic therapy in patients with functioning kidneys, and it demonstrated that ultrafiltration removes a larger volume of fluid and is associated with a greater reduction in 90-day resource utilisation compared to diuretic therapy.
- 67. ACUTE DECOMPENSATED HEARTFAILURE MANAGEMENT OF PATIENTS WITH ACUTE HEART FAILURE
- 68. ACUTE DECOMPENSATED HEARTFAILURE INITIAL MANAGEMENT OF A PATIENT WITH ACUTE HEART FAILURE Jessup, M. et al. (2016) 2016 ESC and ACC/AHA/HFSA heart failure guideline update — what is new and why is it important? Nat. Rev. Cardiol. doi:10.1038/nrcardio.2016.134 Modified from Ponikowski, P. et al. 2016 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure: the Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur. Heart J. http://dx.doi.org/10.1093/eurheartj/ehw128 (2016), with permission from Oxford University Press and the ESC
- 69. ACUTE DECOMPENSATED HEARTFAILURE MECHANICAL RESCUE DEVICES AND CHEATS ▸Increase cardiac output by unnatural means: ▸LVAD ▸ECMO ▸Increase the pacemaker rate (60-90 increase of CO by 30%) ▸Decrease the organism's demand for cardiac output ▸Hypothermia ▸Paralysis/sedation
- 70. ACUTE DECOMPENSATED HEARTFAILURE BRIDGING THERAPY TO HEART TRANSPLANT ?
- 71. TEXT OPIATES ▸Opiates relieve dyspnoeaand anxiety. ▸In AHF, routine use of opiates is not recommended ▸only be cautiously considered in patients with severe dyspnoea, mostly with pulmonary oedema. ▸Dose-dependent side effects ▸nausea, hypotension, bradycardia and respiratory depression (potentially increasing the need for invasive ventilation). ▸There are controversies regarding the potentially elevated mortality risk in patients receiving morphine Iakobishvili et all, Use of intravenous morphine for acute decompensated heart failure in patients with and without acute coronary syndromes. Acute Card Care 2011;13:76–80. PeacockWF.ett all.Morphine and outcomes in acute decompensated heart failure: an ADHERE analysis.Emerg Med J 2008;25:205–209.
- 72. ACUTE DECOMPENSATED HEARTFAILURE DEVICE THERAPY - RRT ▸Renal Replacement Therapy - routine use of ultrafiltration is not recommended ▸Criteria for initiation of renal replacement therapy in patients with refractory volume overload: ▸oliguria unresponsive to fluid resuscitation measures, ▸severe hyperkalaemia (K+ >6.5 mmol/L), ▸severe acidaemia (pH <7.2), ▸serum urea level >25 mmol/L (150 mg/dL) and ▸serum creatinine >300 µmol/L (>3.4 mg/dL)
- 73. ACUTE DECOMPENSATED HEARTFAILURE DEVICE THERAPY - MECHANICAL ASSIST DEVICES ▸Intra-aortic balloon pump ▸in cardiac shock ▸otherwise no good evidence ▸IABP did not improve outcomes in patients suffering from AMI and cardiogenic shock - (IABP-SHOCK II trial) ▸Left Ventricular assist devices (LVAD) ▸(MCS) may be used as a ‘bridge to decision’ or longer term in selected patients Thiele H. et all.Intra-aortic balloon counterpulsation in acute myocardial infarction complicated by cardiogenic shock (IABP-SHOCK II): final 12 month results of a randomised, open-label trial. Lancet 2013 38
- 74. ACUTE DECOMPENSATED HEARTFAILURE OTHER INTERVENTIONS ▸In patients with AHF and pleural effusion, pleurocentesis with fluid evacuation may be considered if feasible in order to alleviate dyspnoea. ▸In ascites, ascitic paracentesis with fluid evacuation may be considered in order to alleviate symptoms. ▸reduction in intra-abdominal pressure, ▸partially normalizes the transrenal pressure gradient, thus improving renal filtration.
- 75. ACUTE DECOMPENSATED HEARTFAILURE DISPOSITION ▸The criteria for ICU/CCU admission include any of the following: ▸ need for intubation (or already intubated) ▸ signs/symptoms of hypoperfusion ▸ oxygen saturation (SpO2) <90% (despite supplemental oxygen) ▸ use of accessory muscles for breathing, respiratory rate >25/min ▸ heart rate <40 or >130 bpm, SBP <90 mmHg.
- 76. ACUTE DECOMPENSATED HEARTFAILURE CLINICAL VIGNETTE - OUTCOME OF YOUR PATIENT ▸The middle-aged man with hypertensive decompensated heart failure with acute pulmonary oedema, was started immediately on BiPAP to support his breathing, and he responded well. Bedside pulmonary ultrasound showed B-lines, confirming the diagnosis of pulmonary oedema. He was started on a high-dose nitroglycerin drip, which resulted in a significant improvement in his respiratory symptoms. He received IV diuresis and was admitted to the ICU for further management.
- 77. TEXT TAKE HOME MESSAGE- BE A CHAMP
- 78. USEFUL SCRIPTURE ▸ EBMEDICINEAcute Decompensated Heart Failure: New Strategies for Improving Outcomes May 2017 ▸ 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC)Eur Heart J (2016) 37 (27): 2129-2200
Editor's Notes
- #12 Acute heart failure is defined as new-onset or worsening of symptoms and signs of HF,5 often requiring rapid escalation of therapy and hospital admission. The clinical presentation of AHF typically includes symptoms or signs related to congestion and volume overload rather than to hypoperfusion.7 Since congestion plays a central role for the vast majority of AHF cases, understanding of the underlying pathophysiological mechanisms related to congestion is essential for treating AHF patients.8 More importantly, the level of congestion and the number of congested organs have prognostic relevance in HF patients
- #14 The evaluation of the patient in the ED with possible AHFS includes history, physical examination, chest radiography, 12-lead ECG, cardiac troponin testing (I or T), electrolytes, and a complete blood cell count. The chest radiograph remains a cornerstone for diagnostic testing, but can lack signs of congestion in over 15% of patients, thus limiting its ability as a screening tool.24 I It is recommended that initial diagnosis of AHF should be based on a thorough history assessing symptoms, prior cardiovascular history and potential cardiac and non-cardiac precipitants, as well as on the assessment of signs/symptoms of congestion and/or hypoperfusion by physical examination and further confirmed by appropriate additional investigations such as ECG, chest X-ray, laboratory assessment (with specific biomarkers) and echocardiography.
- #16 AHF may present as a first occurrence (de novo) or, more frequently, as a consequence of acute decompensation of chronic HF, and may be caused by primary cardiac dysfunction or precipitated by extrinsic factors, often in patients with chronic HF. Acute myocardial dysfunction (ischaemic, inflammatory or toxic), acute valve insufficiency or pericardial tamponade are among the most frequent acute primary cardiac causes of AHF.
- #23 Clinical classification can be based on bedside physical examination in order to detect the presence of clinical symptoms/signs of congestion (‘wet’ vs. ‘dry’ if present vs. absent) and/or peripheral hypoperfusion (‘cold’ vs. ‘warm’ if present vs. absent) (Figure 12.1).514,515 The combination of these options identifies four groups: warm and wet (well perfused and congested) —most commonly present; cold and wet (hypoperfused and congested); cold and dry (hypoperfused without congestion); and warm and dry (compensated, well perfused without congestion). This classification may be helpful to guide therapy in the initial phase and carries prognostic information.510,5
- #28 Radiological features of acute pulmonary oedema There are two distinct radiological phases. The interstitial phase is the fluid filling up spaces between acini; the alveolar phase is where that fluid floods the air spaces. Both phases tend to appear at the same time in ICU patients, at least in the context of fluid overload and heart failure. • Interstitial pulmonary oedema may develop first. • Small pulmonary vessels lose their definition on the radiograph; blurring occurs. This can be mistaken for something • Peribronchial cuffing occurs: the blood vessels which follow the bronchi become engorged, and thus causes a "cuffed" appearance. These cuffs are usually the most prominent around the hila. • Kerley B lines may appear - these are linear shadows created by collections of septal fluid; they tend to be most prominent near the peripheries of the lungs, because the fissures are seen side-on. • Thickening of fissures also occurs for the same reason; think of them as really big Kerley lines. • Pleural effusions may form • "Bat Wing" oedema is alveolar oedema in a non-gravity-dependent distribution, and is usually seen in hyper-acute heart failure, eg. if there is acute mitral incompetence due to papillary muscle rupture.
- #39 The natriuretic peptides b-type natriuretic peptide (BNP) and N-terminal (NT)-proBNP have demonstrated diagnostic utility in this patient population when clinical uncertainty remains after initial history, physical examination, and chest radiography. These biomarkers are generated from a prohormone released from cardiac myocytes in response to ventricular dilatation and pressure overload.25,–,27 After release from the cardiac myocyte, the prohormone proBNP is cleaved into BNP, which is metabolically active, and NT-proBNP, which is metabolically inactive. Both BNP and NT-proBNP are elevated in AHFS and the magnitude of marker elevation is correlated with severity of illness. Using a cutoff of 100 pg/mL, BNP had a sensitivity, specificity, negative predictive, and positive predictive value of 90%, 76%, 79%, and 89%, respectiv ely.In this capacity, BNP is highly useful to exclude AHFS The natriuretic peptides are particularly good at ruling out AHFS; the negative likelihood ratio of BNP at 100 pg/mL is 0.13
- #47 Identification of precipitants/causes leading to decompensation that needs urgent management The next step should comprise the identification of major precipitants/causes leading to decompensation, which should be managed urgently to avoid further deterioration (Figure 12.2). These include the following: Identification of acute aetiologies/precipitants with subsequent initiation of specific treatments should be done within the immediate phase of AHF management (initial 60–120 min) (Figure 12.2). • Acute coronary syndrome. Patients presenting with ACS should be managed according to the ESC guidelines on non-ST elevation ACS (NSTE-ACS) and STEMI.114,535 Coexistence of these two clinical conditions (ACS and AHF) always identifies a very-high-risk group where an immediate (i.e. <2 h from hospital admission in patients with NSTEMI, analogous to STEMI management) invasive strategy with intent to perform revascularization is recommended, irrespective of ECG or biomarker findings.114,535 See below for patients presenting with persistent haemodynamic instability due to mechanical ACS complication. • Hypertensive emergency. AHF precipitated by rapid and excessive increase in arterial blood pressure typically manifests as acute pulmonary oedema. A prompt reduction in blood pressure should be considered as a primary therapeutic target and initiated as soon as possible. Aggressive blood pressure reduction (in the range of 25% during the first few hours and cautiously thereafter) with i.v. vasodilators in combination with loop diuretics is recommended.317,536,537 • Rapid arrhythmias or severe bradycardia/conduction disturbance. Severe rhythm disturbances in patients with AHF and unstable conditions should be corrected urgently with medical therapy, electrical cardioversion or temporary pacing260,316,389 (see also Section 10.1 for AF management). Electrical cardioversion is recommended if an atrial or ventricular arrhythmia is thought to be contributing to the patient's haemodynamic compromise in order to restore sinus rhythm and improve the patient's clinical condition. Patients with AHF and incessant ventricular arrhythmias present a challenging scenario, as arrhythmias and haemodynamic instability operate in a vicious circle, perpetuating each other. In selected cases, immediate angiography (with resultant revascularization, if needed) and electrophysiological testing with radiofrequency ablation may be considered.260 • Acute mechanical cause underlying AHF. This may present as a mechanical complication of ACS (free wall rupture, ventricular septal defect, acute mitral regurgitation), chest trauma or cardiac intervention, or as acute native or prosthetic valve incompetence secondary to endocarditis, aortic dissection or thrombosis and comprise rare causes of obstruction (e.g. cardiac tumours). Echocardiography is essential for diagnosis, and treatment typically requires circulatory support with surgical or percutaneous intervention. • Acute pulmonary embolism. When acute pulmonary embolism is confirmed as the cause of shock or hypotension, immediate specific treatment is recommended with primary reperfusion either with thrombolysis, catheter-based approach or surgical embolectomy.526 Patients presenting with acute pulmonary embolism should be managed according to the appropriate guidelines.
- #49 A large number of overlapping classifications of AHF based on different criteria have been proposed.510–513 In practice the most useful classifications are those based on clinical presentation at admission, allowing clinicians to identify patients at high risk of complications and to direct management at specific targets, which creates a pathway for personalized care in the AHF setting. In most cases, patients with AHF present with either preserved (90–140 mmHg) or elevated (>140 mmHg; hypertensive AHF) systolic blood pressure (SBP). Only 5–8% of all patients present with low SBP (i.e. <90 mmHg; hypotensive AHF), which is associated with poor prognosis, particularly when hypoperfusion is also present
- #50 Clinical classification can be based on bedside physical examination in order to detect the presence of clinical symptoms/signs of congestion (‘wet’ vs. ‘dry’ if present vs. absent) and/or peripheral hypoperfusion (‘cold’ vs. ‘warm’ if present vs. absent) (Figure 12.1).514,515 The combination of these options identifies four groups: warm and wet (well perfused and congested) —most commonly present; cold and wet (hypoperfused and congested); cold and dry (hypoperfused without congestion); and warm and dry (compensated, well perfused without congestion). This classification may be helpful to guide therapy in the initial phase and carries prognostic information.510,5
- #54 Vasodilators Intravenous vasodilators (Table 12.4) are the second most often used agents in AHF for symptomatic relief; however, there is no robust evidence confirming their beneficial effects. They have dual benefit by decreasing venous tone (to optimize preload) and arterial tone (decrease afterload). Consequently, they may also increase stroke volume. Vasodilators are especially useful in patients with hypertensive AHF, whereas in those with SBP <90 mmHg (or with symptomatic hypotension) they should be avoided. Dosing should be carefully controlled to avoid excessive decreases in blood pressure, which is related to poor outcome. Vasodilators should be used with caution in patients with significant mitral or aortic stenosis.
- #56 Use of an inotrope (Table 12.5) should be reserved for patients with a severe reduction in cardiac output resulting in compromised vital organ perfusion, which occurs most often in hypotensive AHF. Inotropic agents are not recommended in cases of hypotensive AHF where the underlying cause is hypovolaemia or other potentially correctable factors before elimination of these causes. Levosimendan is preferable over dobutamine to reverse the effect of beta-blockade if beta-blockade is thought to be contributing to hypoperfusion.572 However, levosimendan is a vasodilator, thus it is not suitable for treatment of patients with hypotension (SBP <85 mmHg) or cardiogenic shock unless in combination with other inotropes or vasopressors.559,573,574 Inotropes, especially those with adrenergic mechanisms, can cause sinus tachycardia and may induce myocardial ischaemia and arrhythmias, thus ECG monitoring is required. There is long-standing concern that they may increase mortality, which derives from studies in which intermittent or continuous infusions of inotropes were given.559–563,575 In any case, inotropes have to be used with caution starting from rather low doses and up-titrating with close monitoring.
- #57 Digoxin is mostly indicated in patients with AF and rapid ventricular rate (>110 bpm) and given in boluses of 0.25–0.5 mg i.v. if not used previously (0.0625–0.125 mg may be an adequate dose in patients with moderate to severe renal dysfunction). However, in patients with co-morbidities or other factors affecting digoxin metabolism (including other drugs) and/or the elderly, the maintenance dose may be difficult to estimate theoretically, and in this situation it should be established empirically, based on the measurements of digoxin concentration in peripheral blood.
- #58 Cardiogenic shock is defined as hypotension (SBP <90 mmHg) despite adequate filling status with signs of hypoperfusion (Table 12.2). The pathogenetic scenarios of cardiogenic shock range from low-output advanced end-stage chronic HF to acute-onset de novo cardiogenic shock most often caused by STEMI, but also by various aetiologies other than ACS. A patient in cardiogenic shock should undergo immediate comprehensive assessment. ECG and echocardiography are required immediately in all patients with suspected cardiogenic shock. In patients with cardiogenic shock complicating ACS, an immediate coronary angiography is recommended (within 2 h from hospital admission) with an intent to perform coronary revascularization. As a vasopressor, norepinephrine is recommended when mean arterial pressure needs pharmacologic support. Dobutamine is the most commonly used adrenergic inotrope. Levosimendan may also be used in combination with a vasopressor.
- #59 Diuretics are a cornerstone in the treatment of patients with AHF and signs of fluid overload and congestion. Diuretics increase renal salt and water excretion and have some vasodilatory effect. In patients with AHF and signs of hypoperfusion, diuretics should be avoided before adequate perfusion is attained. The initial approach to congestion management involves i.v. diuretics with the addition of vasodilators for dyspnoea relief if blood pressure allows. To enhance diuresis or overcome diuretic resistance, options include dual nephron blockade by loop diuretics (i.e. furosemide or torasemide) with thiazide diuretics or natriuretic doses of MRAs.570,571 However, this combination requires careful monitoring to avoid hypokalaemia, renal dysfunction and hypovolaemia. Data defining optimal dosing, timing and method of delivery are incomplete. In the ‘high-dose’ arm of the DOSE study, administration of furosemide at 2.5 times the previous oral dose resulted in greater improvement in dyspnoea, larger weight change and fluid loss at the cost of transient worsening in renal function.548 In AHF, i.v. furosemide is the most commonly used first-line diuretic. The dose should be limited to the smallest amount to provide adequate clinical effect and modified according to previous renal function and previous dose of diuretics. The initial i.v. dose should be at least equal to the pre-existing oral dose used at home. Consequently, patients with new-onset AHF or those with chronic HF without a history of renal failure and previous use of diuretics may respond to i.v. boluses of 20–40 mg, whereas those with previous use of diuretics usually require higher doses. A bolus of 10–20 mg i.v. torasemide may be considered as an alternative.
- #72 Opiates relieve dyspnoea and anxiety. In AHF, routine use of opiates is not recommended and they may only be cautiously considered in patients with severe dyspnoea, mostly with pulmonary oedema. Dose-dependent side effects include nausea, hypotension, bradycardia and respiratory depression (potentially increasing the need for invasive ventilation). There are controversies regarding the potentially elevated mortality risk in patients receiving morphine
- #73 Renal replacement therapy Ultrafiltration involves the removal of plasma water across a semipermeable membrane in response to a transmembrane pressure gradient. There is no evidence favouring ultrafiltration over loop diuretics as first-line therapy in patients with AHF.571,578 At the present time, routine use of ultrafiltration is not recommended and should be confined to patients who fail to respond to diuretic-based strategies. The following criteria may indicate the need for initiation of renal replacement therapy in patients with refractory volume overload: oliguria unresponsive to fluid resuscitation measures, severe hyperkalaemia (K+ >6.5 mmol/L), severe acidaemia (pH <7.2), serum urea level >25 mmol/L (150 mg/dL) and serum creatinine >300 µmol/L (>3.4 mg/dL). Mechanical assist devices Intra-aortic balloon pump The conventional indications for an intra-aortic balloon pump (IABP) are to support the circulation before surgical correction of specific acute mechanical problems (e.g. interventricular septal rupture and acute mitral regurgitation), during severe acute myocarditis and in selected patients with acute myocardial ischaemia or infarction before, during and after percutaneous or surgical revascularization. There is no good evidence that an IABP is of benefit in other causes of cardiogenic shock (for details see below). Ventricular assist devices Ventricular assist devices and other forms of mechanical circulatory support (MCS) may be used as a ‘bridge to decision’ or longer term in selected patients (see Section 13). Other interventions In patients with AHF and pleural effusion, pleurocentesis with fluid evacuation may be considered if feasible in order to alleviate dyspnoea. In patients with ascites, ascitic paracentesis with fluid evacuation may be considered in order to alleviate symptoms. This procedure, through reduction in intra-abdominal pressure, may also partially normalize the transrenal pressure gradient, thus improving renal filtration.581
- #74 The conventional indications for an intra-aortic balloon pump (IABP) are to support the circulation before surgical correction of specific acute mechanical problems (e.g. interventricular septal rupture and acute mitral regurgitation), during severe acute myocarditis and in selected patients with acute myocardial ischaemia or infarction before, during and after percutaneous or surgical revascularization. There is no good evidence that an IABP is of benefit in other causes of cardiogenic shock (for details see below).
- #75 Other interventions In patients with AHF and pleural effusion, pleurocentesis with fluid evacuation may be considered if feasible in order to alleviate dyspnoea. In patients with ascites, ascitic paracentesis with fluid evacuation may be considered in order to alleviate symptoms. This procedure, through reduction in intra-abdominal pressure, may also partially normalize the transrenal pressure gradient, thus improving renal filtration.
- #78 T